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Blood, Vol. 94 No. 11 (December 1), 1999: pp. 3754-3763

SCL Expression in the Mouse Embryo Detected With a Targeted lacZ Reporter Gene Demonstrates Its Localization to Hematopoietic, Vascular, and Neural Tissues

Andrew G. Elefanty, C. Glenn Begley, Lynne Hartley, Bette Papaevangeliou, and Lorraine Robb

From The Walter and Eliza Hall Institute of Medical Research, the Cooperative Research Centre for Cellular Growth Factors and the Rotary Bone Marrow Research Laboratories, Victoria, Australia.

The helix-loop-helix transcription factor SCL (TAL1) is indispensable for blood cell formation in the mouse embryo. We have explored the localization and developmental potential of cells fated to express SCL during murine development using SCL-lacZ mutant mice in which the Escherichia coli lacZ reporter gene was `knocked in' to the SCL locus. In addition to the hematopoietic defect associated with SCL deficiency, the yolk sac blood vessels in SCLlacZ/lacZ embryos formed an abnormal primary vascular plexus, which failed to undergo subsequent remodeling and formation of large branching vessels. Intraembryonic vasculogenesis in precirculation SCLlacZ/lacZ embryos appeared normal but, in embryos older than embryonic day (E) 8.5 to E9, absolute anemia leading to severe hypoxia precluded an accurate assessment of further vascular development. In heterozygous SCLlacZ/w embryos, lacZ was expressed in the central nervous system, vascular endothelia, and primitive and definitive hematopoietic cells in the blood, aortic wall, and fetal liver. Culture of fetal liver cells sorted for high and low levels of beta  galactosidase activity from SCLlacZ/w heterozygous embryos indicated that there was a correlation between the level of SCL expression and the frequency of hematopoietic progenitor cells.


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